Researchers at Johns Hopkins University have found that parathyroid hormone treatment may effectively address chronic back pain by reversing nerve growth in damaged spinal discs.
A recent study from Johns Hopkins University suggests that parathyroid hormone (PTH), a hormone traditionally used to treat bone loss, may hold the potential to alleviate chronic back pain at its source. Chronic back pain is frequently associated with the deterioration of spinal discs and the vertebral end plates, which are the thin layers of tissue that separate the discs from the vertebrae. When these structures break down, they become porous, allowing nerves that are typically unaffected to enter the spinal center, resulting in persistent discomfort.
Led by Dr. Janet L. Crane, the research indicates that PTH could prevent and even reverse the growth of pain-sensing nerves into damaged areas of the spine. The parathyroid glands naturally produce PTH, which plays a crucial role in regulating calcium levels and bone remodeling. These findings could shift the treatment paradigm for back pain from merely managing symptoms to addressing the underlying causes.
“During spinal degeneration, pain-sensing nerves grow into regions where they normally do not exist. Our findings show that parathyroid hormone can reverse this process by activating natural signals that push these nerves away,” Crane stated in a press release.
Synthetic versions of PTH are already approved for the treatment of osteoporosis. Previous research had suggested that these treatments might also alleviate bone-related pain, but the biological mechanisms behind this effect were not well understood until now.
Using animal models, the Johns Hopkins team discovered that one to two months of PTH treatment resulted in denser and more stable vertebral end plates. More importantly, the treatment stimulated bone-building cells, known as osteoblasts, to produce a protein called Slit3. This protein plays a key role in repelling growing nerve fibers, thereby preventing them from infiltrating sensitive regions of the spine. The researchers confirmed the significance of Slit3 by removing it from mice, which resulted in the loss of the hormone’s pain-relieving effects.
PTH is already approved by the Food and Drug Administration (FDA) for osteoporosis treatment. Some patients receiving PTH for bone density have reported unexpected relief from back pain, a phenomenon this study may help clarify. “Our study suggests that PTH treatment of lower back pain during spinal degeneration may reduce aberrant innervation,” Crane concluded.
The research lays the groundwork for future clinical trials aimed at exploring PTH’s effectiveness as both a disease-modifying and pain-relieving treatment for spinal degeneration. However, the researchers acknowledged several limitations, including the possibility that PTH treatment could impact the central nervous system in ways not fully examined in this study. As the research focused specifically on the Slit3 protein, further studies are necessary to understand how other genetic factors and bone-forming processes might influence spinal nerve growth and pain relief.
The findings of this study were published in the journal Bone Research.